A young woman with palpitations. What med is she on? With what medication is she non-compliant? What management?

 Written by Pendell Meyers

A woman in her 20s with connective tissue disorder and history of aortic root and valve repair presented with palpitations. 

Here is her triage ECG: 

What do you think?

Atrial flutter with 2:1 conduction. The atrial flutter rate is approximately 200 bpm, with 2:1 AV conduction resulting in ventricular rate almost exactly 100 bpm. 

The fact that the atrial flutter rate is 200 bpm (rather than more typical adult rate of ~300 bpm) suggests that the patient must have one or both of the following:

1) enlarged atria ("bigger race track")

2) sodium channel blockade ("slower race car")

Her medication list was reviewed, and flecainide was found. Further history revealed she had new onset atrial flutter soon after her aortic surgery, and was put on flecainide approximately 1 month ago.

What other medication should also be on the med list? 

An AV nodal blocker (to prevent the possibility of 1:1 conduction if the flecainide slows the flutter rate enough to be conducted 1:1).  This could be a beta blocker such as metoprolol, or a calcium channel blocker such as diltiazem.

Metoprolol was also on the medication list.  And so was an appropriate anti-coagulant, since atrial flutter, like fibrillation, can result in thromboembolism and stroke.

But clinical history suggested she is only taking the flecainide, not the metoprolol.

Several minutes later there was a change in the monitor, and she reported increased palpitations:

With the context, this is almost certainly 1:1 flutter. And superimposed subendocardial ischemia pattern, of course.

She was otherwise very stable during this rhythm.

The physicians gave some IV metoprolol and restarted her on home PO metoprolol. Almost immediately after IV metoprolol the rhythm reverted back to 2:1 flutter:

No further 1:1 flutter occurred. She did well.

Smith: there is something missing here!  Patients with atrial flutter/fib who are on flecainide are on flecainide in order to attempt to keep them in sinus rhythm.  This is a "rhythm control" strategy.  Some patients even use intermittent flecainide to self convert if they feel the fib/flutter.  This is called "pill in the pocket" flecainide.  In this case, we can tell that the patient is taking her flecainide because of the slow atrial rate.  So that flecainide is not doing its job!!  If I saw this patient in the ED, I would electrically cardiovert back to sinus rhythm.  It is possible that her disease has progressed to the point where she cannot be kept in sinus rhythm, but it is worth a try.  She is already anti-coagulated, so that is not an issue.

Flecainide: This is a potentially dangerous Na channel blocker which can cause ventricular dysrhythmias including ventricular fibrillation.  In other words, the main side effect is sudden death!  It should never be initiated by emergency medicine.  Patients must have completely structurally normal hearts.  Aside: I was put on flecainide by my electrophysiologist in order to suppress distressing PVCs (this was when I was doing many night shifts at age 58 -- when I stopped doing nights they went away!  Anecdote?  Causal?  Coincidence?).  Before initiating flecainide, I had a cardiac MRI. Before continuing flecainide, he had me get on a treadmill at full dose and at full exercise (18 minutes) and measured the QRS to be certain that the QRS did not lengthen at all.  Only then was he confident that it would not result in ventricular fibrillation!

Learning Points:

Atrial flutter doesn't have to be 300 bpm atrial rate and 150 bpm ventricular rate (2:1). Several factors can change the atrial rate and the AV conduction pattern. Atrial enlargement and Na channel blockers can decrease the flutter rate. 

Patients on Na channel blockers for atrial flutter should usually be on an AV nodal blocker to prevent 1:1 atrial flutter.

If a patient in on flecainide for atrial flutter/fib, then the care plan is "rhythm control".  If they present to the ED and are on an anticoagulant, or symptoms are less than 12 hours, then go ahead and electrically cardiovert

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MY Comment, by KEN GRAUER, MD (12/24/2023):

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Today's case by Dr. Meyers provides us with the important reminder of what may happen when Flecainide is taken for AFlutter (Atrial Flutter) — without the protective effect of a ß-blocker to prevent 1:1 AV conduction of flutter activity.

• I focus my comments on a number of additional interesting aspects that review of today's case brings up. For clarity and ease of comparison, I've put together in Figure-1 — the 3 serial ECGs in today's case.

QUESTION:

• HOW many additional aspects of today's case did your notice?

Figure-1: To facilitate comparison — I've put the 3 ECGs in today's case together.

Did You Calculate Atrial and Ventricular Rates?

As per Dr. Meyers — Given the context of a patient with known AFlutter since her aortic valve repair — for which she had been taking the Flecainide but not the Metoprolol she was prescribed — ECG #2 almost certainly represented conversion of her AFlutter from 2:1 to 1:1 AV conduction.

• Calculation of atrial and ventricular rates associated with ECG #1 and ECG #2 — adds further support to the supposition that the rhythm in ECG #2 represents 1:1 AFlutter.
• I find use of the Every-Other-Beat Method to be the easiest and fastest way to accurately estimate heart rate when a rhythm is fast and regular. I select a complex in which a part of the QRS either begins or ends on a heavy ECG grid line. I have done this in lead II for each of the 3 tracings shown in Figure-1.
• 
  
• Applying this method to calculate the ventricular rate in ECG #1 — We see that the R-R interval (space between the 2 vertical BLUE lines) — is almost precisely 3 large boxes in duration — which means that the ventricular rate = 300 ÷ 3 = 100/minute.
• Since the PR interval remains constant throughout the tracing — and since we clearly see there are 2 P waves for each QRS — this means that the atrial rate in ECG #1 = 100 X 2 = 200/minute.
• 
  
• PEARL #1: When I am contemplating whether a patient with an SVT that manifests 2:1 AV conduction has been converted to 1:1 AV conduction — I find the fact that the ventricular rate (that had been half the atrial rate when there was 2:1 AV conduction) — is now equal to what the atrial rate was — strongly supports our conclusion that 2:1 conduction is now 1:1. 
• Note in ECG #2 — that 2 QRS complexes now take 3 large boxes to be recorded (space between the 2 vertical RED lines) — which by the Every-Other-Beat Method corresponds to a ventricular rate that is now 200/minute (Half the rate is 300 ÷ 3 = 100/min. X 2 = 200/minute).

Did YOU Notice? — that the ventricular (and therefore also the atrial) rate is now faster in ECG #3 than it was in ECGs #1 and #2?

• By the Every-Other-Beat Method — the R-R interval between each beat (space between the 2 vertical GREEN lines) — is now clearly less than 3 large boxes — which corresponds to a ventricular rate ~110/minute. 
• This means that the atrial rate of flutter activity is now faster than 200/minute (or 110 X 2 ~ 220/minute).
• The "good news" — is that the 1:1 AFlutter that had been present in ECG #2 — has now been converted to 2:1 AFlutter, with resultant reduction in the ventricular rate from 200/minute — to 110/minute.
• 
  
• The above said — WHY did the atrial rate become faster after administration of an IV ß-blocker? I would not have expected the sympathetic attenuation and AV nodal blocking effect of the ß-blocker to speed up atrial activity.
• Rather than the sympathetic attenuation and AV nodal blocking effects of the ß-blocker — perhaps it is simply the fact that this patient's AV node is able to conduct 1:1 at an atrial rate of 200/minute — but not when the atrial rate attains 220/minute.
• Potential Relevance of the Above: IF the atrial rate "slows" slightly and returns to ~200/minute — Will the ß-blocker continue to maintain 2:1 AV conduction?

Additional Management Questions: The patient presented to the ED for palpitations — and was initially in AFlutter with 2:1 AV conduction. She apparently was discharged from the ED in the same rhythm (albeit with the slightly increased atrial rate).

• What is the goal for treatment of this patient's AFlutter? Is this patient a candidate for cardioversion or ablation? (or perhaps she has already been cardioverted one or more times?). And especially if her AFlutter is a permanent rhythm — Is the patient being anticoagulated?

How to Distinguish Between AFlutter vs ATach?

As emphasized by Dr. Meyers — the initial rhythm in today's case is AFlutter with 2:1 AV conduction. To Emphasize:

• PEARL #2: Distinction between AFlutter vs ATach can be difficult from the surface ECG. It's good to appreciate that such distinction is not always possible on the basis of ECG characteristics — since there is overlap in these ECG findings between certain forms of AFlutter vs ATach.
• Untreated AFlutter is in most cases the faster rhythm — with an atrial rate of flutter most often falling within the range of 250-350/minute (most commonly very close to ~300/minute). Although ATach may occasionally attain atrial rates over 250/minute — ATach is usually not this fast. That said — today's case highlights how use of antiarrhythmic medication may account for AFlutter presenting with an atrial rate well under the "expected" 300/minute.
• In theory — typical AFlutter manifests a regular "sawtooth" pattern of atrial activity — whereas ATach most often manifests an isoelectric baseline between atrial deflections. This sawtooth pattern characteristic of AFlutter is seen in ECG #1 in both the inferior leads, and in leads V1 and V2. That said — this morphologic distinction between AFlutter and ATach is not always readily evident.
• The above said, the "good news" — is that initial management in the ED for both AFlutter and ATach is similar. If ablation is contemplated — definitive diagnosis will be made at EP study. (For more on AFlutter — Please check out My Comment in the November 12, 2019 post and the May 1, 2023 post in Dr. Smith's ECG Blog).

WHY is QRS Amplitude so very Tiny in Lead I?

Two entities should immediately come to mind if we see a flat line (or almost a flat line) in lead I:

• Recognition of a flat line ( = zero potential) QRST complex in one of the 3 standard limb leads (ie, in lead I, II or III) — should immediately suggest the possibility of lead misplacement. If the zero potential lead is lead I — this suggests bilateral arm-leg reversal (See Life-In-The-Fast-Lane for details). Reasons I did not think lead reversal was the cause of the lead I appearance in today's 3 ECGs — is that rather than a completely flat line, ECG #2 does manifest a definite QRS complex and T wave. In addition — the QRS complex is upright in the inferior leads, whereas it will typically be predominantly negative with bilateral arm-leg reversal.
• 
  
• PEARL #3: Rather than lead reversal — the reason for the tiny QRST complex in lead I of today's tracings is Schamroth's Sign. As noted in My Comment of the June 17, 2018 post in Dr. Smith's ECG Blog — the presence of an almost “null vector” in standard lead I (ie, P wave, QRS complex and T wave all under 2mm in size) — is highly suggestive of longstanding and severe pulmonary disease. 
• This is relevant to today's case — in that today's patient is a woman in her 20s with a known CTD (Connective Tissue Disease) disorder. A number of potentially severe pulmonary complications that convey higher morbidity and mortality are commonly seen in patients with CTD (Taha and Feteih — NIH, Skills in Rheumatology, 2021).
• 
  
• To Emphasize: Schamroth's Sign is not a common ECG finding in patients with RVH. That said, it is important to recognize this ECG sign when it is present — because of the significant adverse prognostic implications it conveys. (For more on ECG recognition of RVH — See My Comment at the bottom of the page in the March 6, 2022 post of Dr. Smith's ECG Blog).

Finally — Did YOU Recognize the "Technical Misadventures" in Figure-1?

I believe there are several technical misadventures in today's tracings. While these do not alter emergency management of this patient's arrhythmia — They should be noted.

• Lead V6 in ECG #1 looks misplaced. It simply does not make physiologic sense to suddenly see an all-negative QRS complex in this most lateral chest lead.
• The flat line in Lead V6 in ECG #2 indicates a nonfunctional chest lead.
• That lead V6 in ECG #1 was problematic — is confirmed by the predominant positivity that is now seen in ECG #3.
• Speculation: Chest lead electrode placement in women is subject to variation depending on technician practice, patient modesty concerns, and the location and amount of breast tissue that may hinder attaining consistency in lead placement when serial tracings are recorded by different technicians. This could in part account for technical inconsistencies seen in Figure-1.